|
KMID : 0359720080260030224
|
|
Journal of the Korean Neurological Association
2008 Volume.26 No. 3 p.224 ~ p.230
|
|
|
The Effect of Acetylcholine Esterase Inhibitor on Cerebrospinal Fluid β-Amyloid 1-42 and Phosphorylated Tau Protein in Korean Alzheimer’s Disease Patients: Preliminary Study
|
|
Lee Eun-Hui
Youn Young-Chul
Park Kwang-Yeol
Min Ju-Hong
Kwon Oh-Sang
Lee Hyun-Ok
Hong Hyun-Jong
|
|
|
Abstract
|
|
|
Background: Alzheimer’s disease (AD) is characterized by the pathology of amyloid plaques and tau-associated neurofibrillary tangles. Acetylcholine esterase (AChE) transforms the β-amyloid monomer into an oligomer, and increases β-amyloid aggregation in the brain. Increased β-amyloid breaks the cytoskeleton of the brain by hyperphosphorylation of the tau protein. Previous studies support that AChE inhibitor has an inhibitory effect on toxicity of the β-amyloid and phophorylated tau protein. The purpose of this study was to analyze the CSF β-amyloid 1-42 (Aβ1-42) and phosphorylated tau protein in AD and determine their difference depending on whether AChE inhibitor was taken or not.
Methods: Subjects included 16 AD, 14 normal controls, and 15 disease controls. Nine of AD group had taken an AChE inhibitor while the remainder had not. The CSF Aβ1-42 and phosphorylated tau were measured by ELISA.
Results: The CSF Aβ1-42 levels were lower in AD patients than in other groups (p<0.01). We also found increased CSF Aβ1-42 levels in the AChE inhibitor users, compared with non-users.
Conclusions: The level of CSF Aβ1-42 may have a diagnostic value in the patients with cognitive impairments. Also, we may expect the effect of AChE inhibitor on Alzheimer’s pathology by measuring CSF Aβ1-42 levels. Therefore, the level of CSF Aβ1-42 may serve as a biological surrogate marker for AD treatment.
|
|
|
KEYWORD
|
|
|
Alzheimer’s disease, β-Amyloid, Tau protein, Acetylcholine esterase inhibitor
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
  
|